Summary: Berberine, an alkaloid of the protoberberine family, has been shown to have strong positive inotropic and peripheral resistance-lowering effects in dogs with and without heart failure. To determine the acute cardiovascular effects of berberine in humans, 12 patients with refractory congestive heart failure were studied before and during berberine intravenous infusion at rates of 0.02 and 0.2 mg/kg per min for 30 minutes. The lower infusion dose produced no significant circulatory changes, apart from a reduction in heart rate (14%). 14048 -Ribeirrio Preto, SP, Brad sociation properties. These salutary acute effects show that berberine markedly improved cardiac performance in patients with heart failure refractory to conventional medical therapy with digitalis and diuretics. The improvement is probably subsequent to peripheral vasodilatation and to inotropic stimulation. Significant untoward effects appear to be the development of ventricular tachycardia with "torsades de pointes" morphology, detected in 4 patients 1-20 h after the infusion of berberine. This possible association requires further elucidation before the administration of bekrine may be extended to other patients in heart failure.

Summary: A 57-year-old woman developed severe substernal chest pain rddiating to the left arm accompanied hy pallor and marked diaphoresis. These symptoms appeared at rest, lasted 45 minutes, and terminated spntaneously. The patient had been treated for mild hypertension during the last 6 months. An ECG tracing obtained at the beginning of treatment was unremarkable. However, an ECG tracing recorded shortly after the end of the symptoms showed T-wave inversion in all anterior leads. Coronary arteriography was then performed and showed no fixed obstructive coronary artery disease. Nonetheless, a lengthened and constricted myocardial bridging of both the left anterior descending coronary artery and its major diagonal branch was detected. Also, he left anterior descending coronary artery was observed very short. terminating before the cardiac apex. The kft ventricle was hypertrophied. The patient was treated with a beta-blocking agent which eliminated all symptoms.ECG tracing obtained about three months after the onset of the clinical picture was nornial. Our findings suggest that marked myocardial ischemia at rest does occur in patients having myocardial bridges under special circumstances, such as lengthened and constricted myocardial bridging of a short coronary artery which supplies a hypertrophied ventricle. This anomaly should be taken into account as a possible cause of a threatened myocardial infarction, which may be successfully treated with a beta-blocking agent.

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A middle-aged woman with long-term uncontrolled arterial hypertension developed a clinical picture of impending myocardial infarction. A normal coronary arteriogram was obtained. However, left heart catheterization showed a marked increase in left ventricular end-diastolic pressure, while left angiocardiography revealed marked left ventricular hypertrophy. She was successfully treated with a beta-blocking and calcium-antagonist agent. The present case shows that an impending myocardial infarction may occur in patients having normal coronary arteriogram but with left ventricular hypertrophy secondary to arterial hypertension.